A body of opinion suggests that immunological overstimulation of the gastrointestinal and respiratory mucosa is involved in SIDS. The local stimulation of immunoglobulin concentration in the respiratory mucosa is said to be the consequence of an accentuated reaction to a trivial infection (1-4). One hypothesis is that an accentuated airways reactivity plays a key role in the events leading to SIDS and cites the final insult as oxygen lack, low oxygen stores, high oxygen usage and cardiorespiratory failure (5). We hypothesize that hypoxia and antioxidants exacerbate disorders of the paracrine interaction in the airways mucosa leading to overproduction of immunoglobulins. Administration of vitamin E above dietary needs to hypoxic chicks increased the immune response. The effects were considered synergistic in elevated production of immunoglobulins, and in their function as antioxidants (6). The oxygen lack, low oxygen stores, high oxygen usage and cardiorespiratory failure (5) are factors capable of provoking an overstimulated immune response in the respiratory mucosa. When levels of T-helper/inducer cells are maintained in AIDS patients' blood plasma, survival time is extended (7). This paper investigates the role of 1,25 (OH) 2D3 in suppression of T-helper/inducer lymphocyte activity in vitro (8,9,34,36), and the failure of activated pulmonary alveolar macrophages (PAM) to produce sufficient 1,25(OH)2D3 to inhibit beta-cell proliferation before differentiation to immunoglobulin secreting cells (4,36).